Particulate matter 2.5 induces the skin barrier dysfunction and cutaneous inflammation via AhR‐ and T helper 17 cell‐related genes in human skin tissue as identified via transcriptome analysis
Particulate matter (PM2.5) is an environmental pollutant causing skin inflammatory diseases via epidermal barrier damage. However, the mechanism and related gene expression induced by PM2.5 remains unclear. Our aim was to determine the effect of PM2.5 on human skin tissue ex vivo, and elucidate the...
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| Veröffentlicht in: | Experimental dermatology 2023-04, Vol.32 (4), p.547-554 |
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| creator | Kim, Han Bi Choi, Min Gyu Chung, Bo Young Um, Ji Young Kim, Jin Cheol Park, Chun Wook Kim, Hye One |
| description | Particulate matter (PM2.5) is an environmental pollutant causing skin inflammatory diseases via epidermal barrier damage. However, the mechanism and related gene expression induced by PM2.5 remains unclear. Our aim was to determine the effect of PM2.5 on human skin tissue ex vivo, and elucidate the mechanism of T helper 17 cell‐related inflammatory cytokine and skin barrier function. We verified the expression levels of gene in PM2.5‐treated human skin tissue using Quantseq (3′ mRNA‐Seq), and Gene Ontology (GO) terms and protein–protein interaction (PPI) networks were performed. The PM2.5 treatment significantly enhanced the expression of Th 1, 2, 17 and 22 cell‐related genes (cut‐off value: │1.2 │ > fold change and p |
| doi_str_mv | 10.1111/exd.14724 |
| format | Article |
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However, the mechanism and related gene expression induced by PM2.5 remains unclear. Our aim was to determine the effect of PM2.5 on human skin tissue ex vivo, and elucidate the mechanism of T helper 17 cell‐related inflammatory cytokine and skin barrier function. We verified the expression levels of gene in PM2.5‐treated human skin tissue using Quantseq (3′ mRNA‐Seq), and Gene Ontology (GO) terms and protein–protein interaction (PPI) networks were performed. The PM2.5 treatment significantly enhanced the expression of Th 1, 2, 17 and 22 cell‐related genes (cut‐off value: │1.2 │ > fold change and p < 0.05). Most of all, Th17 cell‐related genes are upregulated and those genes are associated with skin epidermal barrier function and Aryl hydrocarbon receptor (AhR), a xenobiotic receptor, pathway. In human keratinocyte cell lines, AhR‐regulated genes (e.g. AhRR, CYP1A1, IL6 and IL36G), Th17 cell‐related genes (e.g. IL17C) and epidermal barrier–related genes (e.g. SPRR2A and KRT71) are significantly increased after PM2.5. In the protein level, the secretion of IL‐6 and IL‐36G was increased in human skin tissue following PM2.5 treatment, and the expression of SPRR2A and KRT71 was significantly increased. PM2.5 exposure could ruin the skin epidermal barrier function via AhR‐ and Th17 cell‐related inflammatory pathway.</description><identifier>ISSN: 0906-6705</identifier><identifier>EISSN: 1600-0625</identifier><identifier>DOI: 10.1111/exd.14724</identifier><identifier>PMID: 36471583</identifier><language>eng</language><publisher>Denmark: Wiley Subscription Services, Inc</publisher><subject>aryl hydrocarbon receptor (AhR) ; Cell lines ; Cornified Envelope Proline-Rich Proteins - genetics ; Cytochrome P450 ; epidermal barrier ; Gene expression ; Gene Expression Profiling ; Genes ; Helper cells ; Humans ; Inflammation - genetics ; Inflammation - metabolism ; Inflammatory diseases ; Interleukin 6 ; Lymphocytes T ; Particulate matter ; Particulate Matter - toxicity ; particulate matter 2.5 (PM2.5) ; Proteins ; Receptors, Aryl Hydrocarbon - genetics ; Receptors, Aryl Hydrocarbon - metabolism ; Skin - immunology ; Skin diseases ; Th17 cell ; Th17 Cells - metabolism ; transcriptome analysis ; Transcriptomes</subject><ispartof>Experimental dermatology, 2023-04, Vol.32 (4), p.547-554</ispartof><rights>2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</rights><rights>2023 John Wiley & Sons A/S</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3534-c356523bf9fb69592ad5dcb36a95066456ac513de45fb0da3b67eb7c34c98e203</citedby><cites>FETCH-LOGICAL-c3534-c356523bf9fb69592ad5dcb36a95066456ac513de45fb0da3b67eb7c34c98e203</cites><orcidid>0000-0001-5846-0008 ; 0000-0003-3190-7505 ; 0000-0003-4512-8668 ; 0000-0003-2410-8967 ; 0000-0002-2795-0140 ; 0000-0002-1523-6951 ; 0000-0003-2044-199X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fexd.14724$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fexd.14724$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36471583$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Han Bi</creatorcontrib><creatorcontrib>Choi, Min Gyu</creatorcontrib><creatorcontrib>Chung, Bo Young</creatorcontrib><creatorcontrib>Um, Ji Young</creatorcontrib><creatorcontrib>Kim, Jin Cheol</creatorcontrib><creatorcontrib>Park, Chun Wook</creatorcontrib><creatorcontrib>Kim, Hye One</creatorcontrib><title>Particulate matter 2.5 induces the skin barrier dysfunction and cutaneous inflammation via AhR‐ and T helper 17 cell‐related genes in human skin tissue as identified via transcriptome analysis</title><title>Experimental dermatology</title><addtitle>Exp Dermatol</addtitle><description>Particulate matter (PM2.5) is an environmental pollutant causing skin inflammatory diseases via epidermal barrier damage. However, the mechanism and related gene expression induced by PM2.5 remains unclear. Our aim was to determine the effect of PM2.5 on human skin tissue ex vivo, and elucidate the mechanism of T helper 17 cell‐related inflammatory cytokine and skin barrier function. We verified the expression levels of gene in PM2.5‐treated human skin tissue using Quantseq (3′ mRNA‐Seq), and Gene Ontology (GO) terms and protein–protein interaction (PPI) networks were performed. The PM2.5 treatment significantly enhanced the expression of Th 1, 2, 17 and 22 cell‐related genes (cut‐off value: │1.2 │ > fold change and p < 0.05). Most of all, Th17 cell‐related genes are upregulated and those genes are associated with skin epidermal barrier function and Aryl hydrocarbon receptor (AhR), a xenobiotic receptor, pathway. In human keratinocyte cell lines, AhR‐regulated genes (e.g. AhRR, CYP1A1, IL6 and IL36G), Th17 cell‐related genes (e.g. IL17C) and epidermal barrier–related genes (e.g. SPRR2A and KRT71) are significantly increased after PM2.5. In the protein level, the secretion of IL‐6 and IL‐36G was increased in human skin tissue following PM2.5 treatment, and the expression of SPRR2A and KRT71 was significantly increased. PM2.5 exposure could ruin the skin epidermal barrier function via AhR‐ and Th17 cell‐related inflammatory pathway.</description><subject>aryl hydrocarbon receptor (AhR)</subject><subject>Cell lines</subject><subject>Cornified Envelope Proline-Rich Proteins - genetics</subject><subject>Cytochrome P450</subject><subject>epidermal barrier</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Genes</subject><subject>Helper cells</subject><subject>Humans</subject><subject>Inflammation - genetics</subject><subject>Inflammation - metabolism</subject><subject>Inflammatory diseases</subject><subject>Interleukin 6</subject><subject>Lymphocytes T</subject><subject>Particulate matter</subject><subject>Particulate Matter - toxicity</subject><subject>particulate matter 2.5 (PM2.5)</subject><subject>Proteins</subject><subject>Receptors, Aryl Hydrocarbon - genetics</subject><subject>Receptors, Aryl Hydrocarbon - metabolism</subject><subject>Skin - immunology</subject><subject>Skin diseases</subject><subject>Th17 cell</subject><subject>Th17 Cells - metabolism</subject><subject>transcriptome analysis</subject><subject>Transcriptomes</subject><issn>0906-6705</issn><issn>1600-0625</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1u1DAUhS0EokNhwQsgS2zoYqZ2HNvNsuoPIFUCoSKxi27sG8YlcQb_ALPjEXgonoQnwWkKCyS8sKV7vnuu7UPIU842vKxj_GY3vNZVfY-suGJszVQl75MVa5haK83kAXkU4w1jXAstH5IDoWrN5YlYkZ9vISRn8gAJ6QgpYaDVRlLnbTYYadoijZ-cpx2E4Ipo97HP3iQ3eQreUpMTeJxyLC39AGPxmKUvDujp9t2v7z9uqWu6xWFX2rmmBoeh1APOMy39iB7nZrrNI_hlWHIxZqRQ6hZ9cr0r4GyZAvhogtulaSy6h2EfXXxMHvQwRHxydx6S95cX12ev1ldvXr4-O71aGyFFPe9KVqLrm75TjWwqsNKaTihoJFOqlgqM5MJiLfuOWRCd0thpI2rTnGDFxCF5sfjuwvQ5Y0zt6OL8nOUH2kqXELSWoiro83_QmymHct-ZakTNuah1oY4WyoQpxoB9uwtuhLBvOWvnaNsSbXsbbWGf3TnmbkT7l_yTZQGOF-CrG3D_f6f24sP5YvkbW1-yRg</recordid><startdate>202304</startdate><enddate>202304</enddate><creator>Kim, Han Bi</creator><creator>Choi, Min Gyu</creator><creator>Chung, Bo Young</creator><creator>Um, Ji Young</creator><creator>Kim, Jin Cheol</creator><creator>Park, Chun Wook</creator><creator>Kim, Hye One</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-5846-0008</orcidid><orcidid>https://orcid.org/0000-0003-3190-7505</orcidid><orcidid>https://orcid.org/0000-0003-4512-8668</orcidid><orcidid>https://orcid.org/0000-0003-2410-8967</orcidid><orcidid>https://orcid.org/0000-0002-2795-0140</orcidid><orcidid>https://orcid.org/0000-0002-1523-6951</orcidid><orcidid>https://orcid.org/0000-0003-2044-199X</orcidid></search><sort><creationdate>202304</creationdate><title>Particulate matter 2.5 induces the skin barrier dysfunction and cutaneous inflammation via AhR‐ and T helper 17 cell‐related genes in human skin tissue as identified via transcriptome analysis</title><author>Kim, Han Bi ; Choi, Min Gyu ; Chung, Bo Young ; Um, Ji Young ; Kim, Jin Cheol ; Park, Chun Wook ; Kim, Hye One</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3534-c356523bf9fb69592ad5dcb36a95066456ac513de45fb0da3b67eb7c34c98e203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>aryl hydrocarbon receptor (AhR)</topic><topic>Cell lines</topic><topic>Cornified Envelope Proline-Rich Proteins - genetics</topic><topic>Cytochrome P450</topic><topic>epidermal barrier</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Genes</topic><topic>Helper cells</topic><topic>Humans</topic><topic>Inflammation - genetics</topic><topic>Inflammation - metabolism</topic><topic>Inflammatory diseases</topic><topic>Interleukin 6</topic><topic>Lymphocytes T</topic><topic>Particulate matter</topic><topic>Particulate Matter - toxicity</topic><topic>particulate matter 2.5 (PM2.5)</topic><topic>Proteins</topic><topic>Receptors, Aryl Hydrocarbon - genetics</topic><topic>Receptors, Aryl Hydrocarbon - metabolism</topic><topic>Skin - immunology</topic><topic>Skin diseases</topic><topic>Th17 cell</topic><topic>Th17 Cells - metabolism</topic><topic>transcriptome analysis</topic><topic>Transcriptomes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Han Bi</creatorcontrib><creatorcontrib>Choi, Min Gyu</creatorcontrib><creatorcontrib>Chung, Bo Young</creatorcontrib><creatorcontrib>Um, Ji Young</creatorcontrib><creatorcontrib>Kim, Jin Cheol</creatorcontrib><creatorcontrib>Park, Chun Wook</creatorcontrib><creatorcontrib>Kim, Hye One</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental dermatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Han Bi</au><au>Choi, Min Gyu</au><au>Chung, Bo Young</au><au>Um, Ji Young</au><au>Kim, Jin Cheol</au><au>Park, Chun Wook</au><au>Kim, Hye One</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Particulate matter 2.5 induces the skin barrier dysfunction and cutaneous inflammation via AhR‐ and T helper 17 cell‐related genes in human skin tissue as identified via transcriptome analysis</atitle><jtitle>Experimental dermatology</jtitle><addtitle>Exp Dermatol</addtitle><date>2023-04</date><risdate>2023</risdate><volume>32</volume><issue>4</issue><spage>547</spage><epage>554</epage><pages>547-554</pages><issn>0906-6705</issn><eissn>1600-0625</eissn><abstract>Particulate matter (PM2.5) is an environmental pollutant causing skin inflammatory diseases via epidermal barrier damage. However, the mechanism and related gene expression induced by PM2.5 remains unclear. Our aim was to determine the effect of PM2.5 on human skin tissue ex vivo, and elucidate the mechanism of T helper 17 cell‐related inflammatory cytokine and skin barrier function. We verified the expression levels of gene in PM2.5‐treated human skin tissue using Quantseq (3′ mRNA‐Seq), and Gene Ontology (GO) terms and protein–protein interaction (PPI) networks were performed. The PM2.5 treatment significantly enhanced the expression of Th 1, 2, 17 and 22 cell‐related genes (cut‐off value: │1.2 │ > fold change and p < 0.05). Most of all, Th17 cell‐related genes are upregulated and those genes are associated with skin epidermal barrier function and Aryl hydrocarbon receptor (AhR), a xenobiotic receptor, pathway. In human keratinocyte cell lines, AhR‐regulated genes (e.g. AhRR, CYP1A1, IL6 and IL36G), Th17 cell‐related genes (e.g. IL17C) and epidermal barrier–related genes (e.g. SPRR2A and KRT71) are significantly increased after PM2.5. In the protein level, the secretion of IL‐6 and IL‐36G was increased in human skin tissue following PM2.5 treatment, and the expression of SPRR2A and KRT71 was significantly increased. PM2.5 exposure could ruin the skin epidermal barrier function via AhR‐ and Th17 cell‐related inflammatory pathway.</abstract><cop>Denmark</cop><pub>Wiley Subscription Services, Inc</pub><pmid>36471583</pmid><doi>10.1111/exd.14724</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-5846-0008</orcidid><orcidid>https://orcid.org/0000-0003-3190-7505</orcidid><orcidid>https://orcid.org/0000-0003-4512-8668</orcidid><orcidid>https://orcid.org/0000-0003-2410-8967</orcidid><orcidid>https://orcid.org/0000-0002-2795-0140</orcidid><orcidid>https://orcid.org/0000-0002-1523-6951</orcidid><orcidid>https://orcid.org/0000-0003-2044-199X</orcidid></addata></record> |
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| ispartof | Experimental dermatology, 2023-04, Vol.32 (4), p.547-554 |
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| subjects | aryl hydrocarbon receptor (AhR) Cell lines Cornified Envelope Proline-Rich Proteins - genetics Cytochrome P450 epidermal barrier Gene expression Gene Expression Profiling Genes Helper cells Humans Inflammation - genetics Inflammation - metabolism Inflammatory diseases Interleukin 6 Lymphocytes T Particulate matter Particulate Matter - toxicity particulate matter 2.5 (PM2.5) Proteins Receptors, Aryl Hydrocarbon - genetics Receptors, Aryl Hydrocarbon - metabolism Skin - immunology Skin diseases Th17 cell Th17 Cells - metabolism transcriptome analysis Transcriptomes |
| title | Particulate matter 2.5 induces the skin barrier dysfunction and cutaneous inflammation via AhR‐ and T helper 17 cell‐related genes in human skin tissue as identified via transcriptome analysis |
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